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OJHAS Vol. 10, Issue 3:
(Jul-Sep 2011) |
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| Psychosocial and Biological Factors Contributing
to Body Weight Gain in Schizophrenia |
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Shae-Leigh C.
Vella, Graduate School of Medicine, University of Wollongong, New South Wales,
Australia 2522,
Nagesh
B. Pai, Illawarra Health and
Medical Research Institute, Graduate School of Medicine, University of Wollongong, New South Wales,
Australia 2522 |
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Address for Correspondence |
Graduate School of Medicine,
University of Wollongong,
New South Wales,
Australia 2522
E-mail:
vella@uow.edu.au |
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Vella SC, Pai NB. Psychosocial and Biological Factors Contributing
to Body Weight Gain in Schizophrenia. Online J Health Allied Scs.
2011;10(3):1 |
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Submitted: Sep 20,
2011; Accepted: Oct 30, 2011; Published: Nov 15, 2011 |
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| Abstract: |
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Overweight and obesity
are frequently reported to be a significant issue
in schizophrenia resulting in the inherent complications of these disorders.
Body weight gain also commonly results from treatment with the most
tolerable and efficacious pharmacological treatments, second-generation
antipsychotics. However there are numerous other factors that contribute
to increased body mass in individuals with schizophrenia prior to the
initiation of treatment. With prior research indicating that individuals
with schizophrenia have higher rates of overweight and obesity before
treatment. Therefore this article provides a
review of pertinent issues associated with body weight gain in schizophrenia
in an attempt to delineate the impact of both the disease and treatment
upon body weight gain. The results of the review indicate that body
weight gain in schizophrenia occurs from both psychosocial and biological
factors that are further compounded by antipsychotic treatment.
The article concludes with recommendations for future research.
Key Words:
Body weight gain; Psychosocial factors; Biological factors; Schizophrenia;
Overweight; Obesity
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The relationship between
schizophrenia and increased body weight was identified prior to the
advent of the first antipsychotics to treat the disease.[1] This association
was first described in the early 1900’s in the writings of Emil Kraepelin
on the disorder then termed ‘dementia praecox’; the first nomenclature
of schizophrenia symptomology.[1]
Epidemiologically it
is also evident that individuals who suffer from schizophrenia have
higher rates of overweight and obesity in comparison to the general
population.[2,3] A study conducted by Thakore and colleagues [4] found
that both drug-naive and drug-free patients with schizophrenia had higher
BMI’s and waist to hip ratios than age and sex matched controls.
After the introduction
of the first conventional antipsychotic chlorpromazine, in the 1950’s
body weight gain (BWG) as a side effect of treatment was reported.[1]
However BWG was not viewed as one of the most detrimental side effects
due to conventional antipsychotics having other serious side effects,
such as extrapyramidal symptoms, and inducing significantly less BWG
than second generation antipsychotics (SGA).
Although SGA have superior
tolerability and efficacy in comparison to conventional neuroleptic
treatment [5] they commonly induce clinically significant BWG.[6] That is
an increase in body weight that is ≥7% of the individual’s body weight at the
initiation of treatment.[6]
Even though the challenge
of increased body mass of individuals with schizophrenia proportionate
to the general population has been identified for more than a century;
there is relatively scarce literature on the issue relative to the scope
and consequences of the problem. In regards to SGA-induced BWG there
has been a plethora of research. The issue of BWG in schizophrenia is
complex and multi-faceted resulting not only from treatment but also
from the disease itself in addition to the social and cultural environment.
Therefore this article attempts to further clarify the means by which
BWG occurs in schizophrenia.
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The Genesis of
Body Weight Gain & the Consequences |
An increase in body
mass or BWG generally results from a caloric intake that is higher than
the expended energy rate. Energy is expended through the basal metabolic
rate, thermogenesis and physical activity.[3] BWG as a result
of SGA treatment is thought to result from the same genesis as BWG generally.
Within the general population it has been found that even fidgeting combined
with exercises of daily living excluding physical activity is enough to provide
sedentary individuals with a protective barrier against obesity.[7]
An increase in body
weight can result in overweight and obesity and the inherent complications
of these disorders. Namely, metabolic syndromes such as type II diabetes,
cardiovascular disease, hypotension and some forms of cancer.[3] In
addition to the physical toll of overweight and obesity these disorders
also incur a psychological toll. Reducing self-esteem and body image
and leading to greater social deprivation than what the patient is already
experiencing due to schizophrenia symptomology.[3]
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Innate Nature
of Schizophrenia |
One of the most obvious
causal mechanisms that may predispose individuals with schizophrenia
to body weight changes is the innate nature of the illness. Specifically
the cognitive impairment that results from psychosis and the motivational
impact of negative symptomology such as flattened affect may induce
poor lifestyle choices.[3,8] That is unhealthy dietary choices, substance
use / abuse and decreased levels of physical activity. These symptoms
also promote social isolation leading to fewer opportunities for activity
and thus reduced energy expenditure.
In recent times there
has been a proliferation in the number of individuals in the general
population suffering from overweight and obesity.[3] This increase
is thought to have resulted from the influence of an obesigenic environment
evident in industrialised societies. That is an immense increase in
access to high calorie convenience food coupled with reduced opportunities
for physical activity due to labour saving devices, sedentary occupations
and inactive past times.
Furthermore social
deprivation and exclusion are thought to be a causal mechanism that
can contribute to the onset of schizophrenia as well as being maintained
through the nature of the illness [9]. A component of social deprivation
is socio-economic status (SES); which directly affects body weight by
mediating the availability of healthy food choices along with knowledge
of healthy lifestyle factors. Therefore it is not surprising that this
increase in overweight and obesity is also apparent in individuals suffering
from schizophrenia.
Although there is not
a great deal of research on the diets of individuals with schizophrenia
the existing evidence indicates an exaggerated predilection for a diet
of palatable foodstuffs.[2] Palatable foods are those that induce cravings
for consumption (i.e. lollies); and when consumed evoke pleasure and
positive affective states. As oppose to non-palatable foods such as
broccoli. Specifically individuals with schizophrenia have preference
for a diet high in convenience foods that are high in saturated fat
and carbohydrates and low in fibre, such as that provided by fruit and
vegetables.[3]
Furthermore there is
strong correlational evidence to suggest that a diet high in sugar and
saturated fat produces poorer illness outcomes in individuals suffering
from schizophrenia.[10] Whereas the consumption of pulses resulted
in better illness outcomes; that is less hospitalisations and less social
impairment.[10] Thus individuals in developing nations consuming a
non-westernised diet and without access to convenience foodstuffs fair
better than individuals with schizophrenia in industrialised countries.[2,10]
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Inherent Metabolic
Disadvantage |
Metabolic syndrome
is a group of disorders consisting of obesity, glucose intolerance,
insulin resistance and dyslipidaemias that are highly related to the
occurrence of type II diabetes mellitus and cardiovascular disease.[4] It
has also been suggested that individuals that are suffering from schizophrenia
have an inherent metabolic disadvantage that predisposes them to the
onset of metabolic syndromes.[2] Additionally it is known that individuals
with schizophrenia have increased rates of metabolic syndromes above
that of the general population.
That is the metabolic
disadvantage does not just result from SGA treatment as reports of glucose
problems in patients with schizophrenia were recorded prior to the advent
of neuroleptic treatments.[4] Elman, Borsook and Lukas [2] have tentatively
proposed that obesity in schizophrenia may partly result from glucose
metabolism issues that are evident in individuals with schizophrenia.
An inverse relationship to what is currently conceptualised.
For example the higher
rates of type II diabetes mellitus maybe a function of the disease and
not the treatment.[2,4] Empirical research has found that first-degree
relatives of individuals with schizophrenia who do not have schizophrenia
themselves have higher rates of type II diabetes than the general population
[4], thus indicating a possible genetic relationship between schizophrenia
and type II diabetes. In fact, current evidence suggests inherent
abnormalities of insulin signalling pathway in schizophrenia.[11]
In addition another
factor that is implicated in the aetiology of schizophrenia is Insulin–like
Growth Factor 1 (IGF-1). IGF-1 is so named due to its similarity to
insulin. According to the neurodevelopmental model of schizophrenia
deficits of IGF-1 affect prenatal and postnatal development acting as
a pathogenesis for schizophrenia.[12] A deficit IGF-1 has also been
implicated in insulin resistance.[13] This is further supported through recent
studies that have found lower levels of IGF-1 in drug naive individuals with
schizophrenia in comparison to age and sex matched controls.[12,13]
Furthermore it has
been demonstrated that obesity has a very strong heritable component
with 45-85% of the variation in BMI is estimated to be accounted for
by genetics.[14] This is similar to the aetiological contribution of genetics to
schizophrenia.[8]
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Neurological
Reward & Inhibition Mechanisms |
Neurological and neuroanatomical
abnormalities beyond the effect of SGA therapy have been implicated
in driving the desire for sweet and fatty foodstuffs in schizophrenia
through reward and inhibition mechanisms. Specifically neuroanatomical
abnormalities have been identified in the reward and reinforcement circuits
in patients with schizophrenia through neuroimaging, preclinical and
clinical studies.[2] In particular, a hyperfunctional state of the
mesolimboic dopaminergic system in schizophrenia may cause motivational reward
system insensitive to palatable food.[2]
This reward deficiency
is further highlighted by the clinical symptomology of the illness namely;
anhedonia, flattened affect and avolition as well as being reflected
in the high co-morbidity for substance abuse disorders.[2] The neurological
abnormalities coupled with these symptoms induce a reward deficit that
requires higher levels of stimulation; sweeter, fattier foodstuffs in
large quantities in order to satisfy the desire or craving.
It is thought that
the same reward and inhibition mechanisms that drive the desire to seek
and consume drugs and alcohol in substance use disorders also mediate
the desire to seek and consume palatable foodstuff. As it has been found
that palatable foods activate the dopaminergic reward system; in addition
it is also evident that chronic consumption of sweet and fatty foods
can alter the dopaminergic reward system.[2,15] This alteration results
in the individual becoming susceptible to over eating and food addiction;
through conditioning processes.
Furthermore both palatable
foods and drugs are known to increase the release of endogenous opiates.[2,15] Although there are limited human studies, the chronic consumption
of palatable food sources can result in neuroadaptations in the opiod
receptors resulting in opiod dependence. Further driving the desire
to seek and consume unhealthy foodstuffs.
This desire to seek
and consume palatable food is further exacerbated by the ability of
the individual to utilise control mechanisms. Studies with both obese
and drug-addicted individuals have indicated increased prefrontal cortex
activation and decreased performance on a cognitive task in response
to food stimuli and drug stimuli, respectively.[2,14] This hypofunctionality
of the prefrontal cortex results in inhibitory control thus leading
to over eating or the consumption of drugs. In addition recently Volkow
and colleagues [15] have found that addiction not only impacts upon
the dopaminergic reward circuits but is also involved
in conditioning or the forming of habits, motivation as well as executive
functioning.
With regards to antipsychotic-induced
BWG in schizophrenia, the neurological mechanisms through which SGA treatment
results in weight gain are yet to be fully elucidated.[16] It is thought
that SGA-induced BWG results primarily from an increase in appetite.[3,16] However it is also postulated that a decrease in energy expenditure
may also contribute to SGA-induced BWG.[3]
That is SGA’s are
known to induce appetite in individuals with schizophrenia; specifically
an appetite for unhealthy foodstuffs.[3] This cumulatively impacts
upon their already existing predilection for palatable foodstuffs and
their predisposition to metabolic syndromes. This further induces neurological
and neuroanatomical changes in individuals with schizophrenia which
may result in food addiction.
In regards to reduced
energy expenditure a common side effect of SGA treatment is sedation. This
sedation may result in a lack of participation in physical activity further
contributing to weight gain.[3]
From the above review
it is apparent that there are numerous factors beyond treatment with
SGA that induce BWG in some individuals with schizophrenia. There is
substantial evidence that individuals’ with schizophrenia are already predisposed
to making poor food choices through the social and cultural environment
and the symptomology of the disease.
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Figure 1: The Cumulative Process of BWG in Schizophrenia
This figure depicts the multiple factors
that can result in BWG in schizophrenia, each of these factors either
emanates from or interacts with the innate nature of schizophrenia resulting
in a cumulative process of BWG |
This is further exacerbated
by neuroanatomical abnormalities evident in some individuals in schizophrenia
that result in a reward deficient and a lack of executive functioning.
Thus through this deficit and conditioning processes individuals become
vulnerable to food addiction. This further strengthens the predilection
for palatable foodstuffs. The effect of a diet of sugary and fatty foodstuffs
is further compounded by the inherent metabolic disadvantage in some
individuals with schizophrenia. These pre-existing factors are further
compounded by SGA treatment resulting in greater amounts of BWG. The
components of this cumulative process of weight gain are illustrated
in figure 1 above.
Although there is strong
empirical and theoretical evidence that each of these factors can contribute
to BWG for some individuals with schizophrenia. It remains less clear
as to which individuals are predisposed to BWG through each of the above
factors. In addition the hypothesized cumulative nature of BWG in schizophrenia
needs to be tested.
Furthermore future
research should also investigate the diets of individuals with schizophrenia
specifically; trying to ascertain individual and illness differences
between individuals with poor and ‘good’ food choices. Such endeavours
could both highlight those that are at an increased risk of BWG as well
as inform lifestyle interventions.
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